Some view sympathetic activation, with its accompanied increased release and diminished reuptake of norepinephrine from myocardial sympathetic nerve terminals, as a rather acute response to circulatory stress. See, e.g., Frantz, “Beta blockade in patients with congestive heart failure,” Postgraduate Medicine, 108(3), 103–118 (2000). Norepinephrine, a catecholamine released by sympathetic nerves, causes an increase in heart rate and inotropy (contractility) and hence cardiac output. Frantz explains that “[i]n a teleological sense, an acute increase in sympathetic drive was advantageous for our ancestors. When they were being pursued by a tiger or bleeding from a wound, increasing heart rate, peripheral tone, and myocardial contractility allowed them to reach safety or maintain central perfusion”. However, chronic sympathetic activation may cause a progressive deterioration in cardiac output. In addition, uncontrollable sympathetic surges can increase the risk of fatal arrhythmia. Thus, sympathetic activation has both beneficial attributes and detrimental attributes. As described below, selective and/or controllable activation of sympathetic neurons may increase beneficial attributes while diminishing detrimental attributes.